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Critical Reviews™ in Immunology
Импакт фактор: 1.404 5-летний Импакт фактор: 3.347 SJR: 0.706 SNIP: 0.55 CiteScore™: 2.19

ISSN Печать: 1040-8401
ISSN Онлайн: 2162-6472

Выпуски:
Том 40, 2020 Том 39, 2019 Том 38, 2018 Том 37, 2017 Том 36, 2016 Том 35, 2015 Том 34, 2014 Том 33, 2013 Том 32, 2012 Том 31, 2011 Том 30, 2010 Том 29, 2009 Том 28, 2008 Том 27, 2007 Том 26, 2006 Том 25, 2005 Том 24, 2004 Том 23, 2003 Том 22, 2002 Том 21, 2001 Том 20, 2000 Том 19, 1999 Том 18, 1998 Том 17, 1997 Том 16, 1996 Том 15, 1995 Том 14, 1994

Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.v23.i4.20
34 pages

Endothelial Responses to Bacterial Toxins in Sepsis

Ulrich Grandel
Department of Internal Medicine, Justus-Liebig-University, 35392 Giessen, Germany
Friedrich Grimminger
Department of Internal Medicine, Justus-Liebig-University, 35392 Giessen, Germany

Краткое описание

The virulence of pathogenic bacteria is critically dependent on their ability to produce toxins that attack eukaryotic target cells. Microbial toxins are either structural components of the bacterial cell wall (endotoxins) or actively secreted proteins (exotoxins). Sepsis and septic shock, which represent major causes of mortality in modern intensive care medicine, are caused by an inadequate inflammatory and immunological host response to bacterial infection. Emerging evidence suggests that the systemic spread of microbial toxins, rather than bacteremia itself, is the crucial event in the pathogenesis of this dramatic dysregulation. The endothelium, with its diversity of physiological functions is a main target of bacterial toxins. The resulting endothelial dysfunction is believed to contribute to the underlying pathomechanisms and the collapse of homeostasis of organ function. In vitro, bacterial toxins induce subtle alterations of endothelial cell function rather than massive cell damage. Furthermore, bacterial toxins targeting endothelial cells severely alter the behavior of extravascular cells and circulating leukocytes via excessive formation of vasoactive mediators and overexpression of adhesion molecules. Research on the effects of microbial toxins on vascular endothelium has broadened our general understanding of microbial strategies to induce organ damage, even in the absence of viable bacteria. Combining antitoxin strategies with antibiotic therapy may prove to be of benefit to patients suffering from bacterial sepsis in the future.


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